An introduction

Cognitive psychology is the scientific investigation of cognition, that is, of all mental abilities: perception, attention, learning, memory, processing of spoken and written language, thinking, reasoning and belief formation (Coltheart, 2002). It assumes that cognition can at least in principle be fully revealed by the scientific method, that is, individual components of mental processes can be identified and understood. These individual components of mind are mental modules, and thus contemporary cognitive psychology often assumes the modularity of mind (Fodor, 1983).

Any theory about any domain of cognition will therefore be a theory about (a) what the modules are of the system by which performance in that domain is accomplished, and (b) what the pathways of communication between these modules of the system are; that is, a theory about the functional architecture of the system. Most cognitive psychologists seek to develop and test such theories by experiments with people who are skilled performers in the relevant cognitive domain. But one can also learn about cognitive systems by studying ways in which they break down after brain damage: and this is the approach known as cognitive neuropsychology. So cognitive neuropsychology is a subfield of cognitive psychology, distinguished by the feature that it studies people with disorders of perception, attention, learning, memory, processing of spoken and written language, thinking, reasoning or belief formation, with the aim of learning more about the normal functional architectures of the cognitive processing systems used to carry out these activities.

Hence, although it is typical for cognitive neuropsychologists to be studying people who have brain damage, these scientists are not studying the brain mechanisms associated with cognitive processes: such study is a different discipline, cognitive neuroscience. Cognitive neuropsychologists are studying the mind rather than the brain (which is why one says that cognitive neuropsychology is a subfield of cognitive psychology, just as cognitive neuroscience - which does study the brain - is a subfield of neuroscience).

This sharp distinction between research on the mind (cognition) and research on the brain is urged by numerous philosophers of mind and cognitive psychologists including Block (1995), Fodor (1999), Marshall (see e.g. Marshall and Gurd, 1996), Morton (1984), Page (2006), Pylyshyn (1980), and Van Orden and Paap (1997), all of whom argue for the view that facts about the brain do not at all constrain the construction of theories of cognition that are expressed in functional or information-processing terms, even if these theories have been constructed from studying the performance of people with cognitive impairments due to brain damage (which is what cognitive neuropsychologists, by definition, do)

Of course, scientists who study cognition might want to do more than build theories about the mechanisms that are just expressed in functional or information-processing terms. They might also want to discover something about the neural bases of these information-processing mechanisms of cognition (which is what cognitive neuroscientists, by my definition, do). Since, as the authors cited in the previous paragraph argue, one can do cognitive neuropsychology successfully without needing to study the neural bases of cognition, the distinction between cognitive neuropsychology and cognitive neuroscience is a valuable one, even if many researchers interested in these matters do both kinds of work. The importance of this distinction is reinforced by the fact that amongst those who believe that knowledge about the brain won’t constrain information-processing theorizing about cognition are some of the most distinguished practitioners of cognitive neuropsychology – John Marshall and John Morton, for example.

The distinction I am drawing here between cognitive neuropsychology and cognitive neuroscience is very well expressed by Scachter (1992, p.56). Re cognitive neuropsychology, he says: "The term cognitive neuropsychology often connotes a purely functional approach to patients with cognitive deficits that does not make use of, or encourage interest in, evidence and ideas about brain systems and processes". But because Schacter is a cognitive neuroscientist as well as a cognitive neuropsychologist, he continues thus: "because I believe that neural constraints can be important for cognitive theorizing, I use the term cognitive neuroscience rather than cognitive neuropsychology".

It is clear that whether neural constraints can or can't be important for cognitive theorizing is a matter of great current controversy: for some recent views on this controversy the reader is referred to a symposium in the journal Cortex (see Coltheart, 2006a, and the commentaries on that target article)

When a person has attained complete skill in some cognitive domain, but then loses some or even all of that skill as a consequence of brain damage, this is known as an acquired disorder of cognition. Some people, however, never succeed in attaining complete skill in some cognitive domain: this is referred to as a developmental disorder of cognition. Developmental cognitive neuropsychologists are those who investigate developmental disorders of cognition with the aim of trying to learn more about how some particular cognitive ability is normally acquired by studying people in whom this acquisition does not proceed normally.

Until about 15 years ago, the domains of cognition with which cognitive neuropsychologists were concerned were basic, well-understood and extensively-investigated aspects of cognition such as perception, attention, learning, memory, and the processing of spoken and written language. But cognitive psychology has also been interested in more complex (and less well-understood) aspects of cognition too, such as thinking, reasoning and belief formation; and there are people who suffer from acquired or developmental disorders of cognition in these higher domains. Why not, then, use studies of such people to try to learn more about these higher-level domains of cognition? One might learn more about how beliefs are normally acquired by studying people with delusions; one might learn more about what underpins empathy by studying people who seem to lack a Theory of Mind. As disorders in these higher-level domains are typically labelled as psychiatric disorders this new kind of cognitive neuropsychology is known as cognitive neuropsychiatry (Ellis, 1998; Coltheart, 2007). But it is crucial to appreciate that just as cognitive neuropsychology, despite its name, is not a kind of neuropsychology but a subfield of cognitive psychology, so it is important to appreciate that cognitive neuropsychiatry, despite its name, is not a kind of psychiatry but another subfield of cognitive psychology.

A very recent development in cognitive neuropsychology is computational cognitive neuropsychology (see e.g. Coltheart, 2006b). This is based on computational modelling of cognition. A computational model of cognition is a computer program which is capable of carrying out some particular cognitive activity such as reading aloud or spelling to dictation or recognizing objects AND which does so by the same processes which, according to some cognitive-psychological theory, are those that human cognizers use when performing this cognitive activity. So the program is an instantiation of the theory, the claim being that a formal description of how the program does the job (for example, a description couched in box-and-arrow notation, or in the notation of production systems) is also the correct formal description of how the mind does the job. Computational cognitive neuropsychology involves damaging the program in various ways and studying whether there are any informative similarities between the impaired performance of the damaged program and the impaired performance of people with acquired disorders of the relevant domain of cognition. This is a rather rigorous way of testing the original cognitive theory. To obtain evidence relevant to the theory, one first has to implement the theory explicitly as a computer program; and then one has to determine whether the symptoms seen in various patients with relevantly disordered cognition can also be exhibited in the behaviour of the program when that program has been damaged. A successful demonstration of this kind is evidence for the theory; inability to mimic a patient’s symptoms by damaging the program is evidence against the theory.

Characteristic features of cognitive neuropsychology

Modular modelling and the assumption of subtractivity

Cognitive neuropsychology shares with the rest of cognitive psychology the aim of discovering what the processing modules of some cognitive system are and what pathways of communication between them exist. That requires cognitive neuropsychology to make the assumption of subtractivity: the assumption that brain damage can subtract modules, or pathways of communication between modules, from the normal system, but cannot add new modules or new pathways. Unless the assumption of subtractivity holds, one cannot make inferences about the functional architecture of the normal system from evidence concerning the functional architecture of a damaged system. For further discussion of the assumption of subtractivity, see Caramazza (1984), Ellis & Young (1996, pp. 16-19) and Coltheart (2001, pp 9-11)

Inferences from double dissociation

One reason that cognitive-neuropsychological research is perennially exciting is that it continually reveals disorders of remarkable selectivity and specificity. Patient KT (McCarthy and Warrington, 1986) was normal at reading aloud pronounceable nonwords (even though he would never have seen these before), but very impaired at reading aloud real words which he would have seen before, when these words disobeyed the spelling-sound rules of English (irregular or exception words). Patient MH (Humphreys & Rumiati, 1998)) could recognize visually presented faces and printed words - but not objects. Patient AC (Coltheart. Inglis, Cupples, Michie, Bates & Budd, 1998) could provide on request any information about objects whose names were spoken to him - except visual information; thus he could say that oysters are edible, dwell in the sea and smell faintly of it, and are silent, but he could not provide any information about whether or not they have any legs, what their general shape is, or what colour they are. Surely such results allow us to infer in a justified manner important things about the functional architectures of the cognitive systems involved in reading, object recognition and comprehension?

They do - provided certain methodological precautions are observed.

Suppose, for example, we came across a stroke patient whose recognition of stimuli in all sensory modalities bar vision was intact; and he was not blind because he could describe well the visual properties of any stimulus he was looking at; yet he could not recognize objects, faces or printed words. No matter how familiar such stimuli were, all looked completely unfamiliar to him. We might infer from this association of three deficits that there is a single visual recognition module that is used for recognizing objects, faces and printed words, damage to this module being the cause of the patient’s symptoms. But there is an alternative and entirely reasonable inference: that there are three separate visual recognition modules, one for each of these classes of stimuli, and that they are located close together in the brain in a region with a single blood supply which the stroke had affected. This illustrates why cognitive neuropsychology does not regard the observation of an association between impairments as offering a secure basis for making inferences about functional architecture.

Suppose now, however, we came across a second stroke patient, one whose recognition of stimuli in all sensory modalities bar vision was intact; and he was not blind because he could describe well the visual properties of any stimulus he was looking at; and he could not recognize objects even though he could recognize faces or printed words. Here we have, not an association, but a dissociation, of deficits: impaired object recognition with intact face and word recognition. Might we not infer from this dissociation that the functional architecture of the visual recognition system includes a module specialized just for object recognition and not used for recognizing faces or printed words?

Such inferences from dissociations however are open to a straightforward objection too. Perhaps there is a single visual recognition module that is used for recognizing objects, faces and printed words, but objects are more difficult for it to recognize than are faces or printed words. If that were so, and the module were partially impaired by brain damage, the module might still be able to accomplish easier tasks (face and word recognition) whilst producing imperfect performance in the task hardest for it (object recognition). This argument makes the data from this patient compatible with two different proposals about the functional architecture of visual recognition.

What the cognitive neuropsychologist wants are data that can be reasonably argued to specifically favour one particular proposal about functional architecture at the expense of competing proposals. Such data cannot be provided by observations of associations or single dissociations, but they can be provided by observations of double dissociations. Suppose a third stroke patient is seen whose recognition of stimuli in all sensory modalities bar vision was intact; and he was not blind because he could describe well the visual properties of any stimulus he was looking at; and he could not recognize faces, even though he could recognize objects and printed words. When this third patient is considered in conjunction with the second patient, just described, we have a double dissociation of deficits: impaired object recognition with intact face recognition in one patient, and the opposite pattern in another. One might infer from the data from these two patients that there is a module dedicated to object recognition and a distinct module dedicated to face recognition. This inference is not open to the objection that can be made to inference from association, and it is not open to the objection which can be made to the inference from single dissociations. That is why cognitive neuropsychologists focus on the study of double dissociations when making inferences about the functional architecture of cognition from patient data.

Of course, no cognitive neuropsychologist would ever claim that it is indubitably the case, given this observed double dissociation, that there must be distinct object and face recognition modules. There are no methods in science that permit inferences of theory from data that are free from doubt (science, including cognitive neuropsychology, isn’t like that). However, inferences from double dissociation have the virtue that they have no consistent intrinsic weaknesses (unlike inferences from association or single dissociation); so these are perfectly reasonable inferences to make. And furthermore, if anyone wishes to dispute the particular functional architecture some theorist has inferred from some double dissociation, it is up to them to propose an alternative architecture which is also compatible with the observed double-dissociation data. Further discussions of the double dissociation method may be found in Shallice (1988, ch 10), Jones (1983), Plaut (1995) and the reply to this by Bullinaria & Chater (1995), McCloskey (2001), and a special issue of the journal Cortex (2003, volume 39, Issue 1) devoted to this topic.

Rejection of the syndrome as a subject of scientific investigation

Figure 1 depicts a rather basic model of the functional architecture of the reading system (Coltheart, Rastle, Perry, Langdon & Ziegler, 2001). At least as far as reading at the single word level is concerned, this is a model of how we recognize print and how we read aloud. Each of the boxes and arrows in the model is motivated, in the sense that if any one of them were deleted from the system, there would be some reading task that skilled readers can do which the system could not do. It follows that if brain damage affected any module or any pathway in the system, some form of reading disorder - some kind of acquired dyslexia - would result. What the actual pattern of preserved and impaired reading abilities would be would vary as a function of which modules or pathways were preserved. and which were impaired. Since the system has 15 components (7 modules and 8 pathways of communication), the number of possible distinct syndromes of acquired dyslexia that could result from damage to one or more components of this quite simple system is \(2^{15}-1 = 32767\) distinct syndromes. This is why cognitive neuropsychologists do not study syndromes such as “apraxia”, “agnosia” or “aphasia” - not even subsyndromes such as “ideomotor apraxia”, “apperceptive agnosia” or “Broca’s aphasia”. No two patients one is likely to see in one’s lifetime will have precisely the same pattern of preserved and impaired processing components of the relevant cognitive system. So there is no sense in grouping patients under syndrome labels, and studying syndromes.

Figure 1:

Emphasis on the study of single cases

Each patient a cognitive neuropsychologist sees will thus almost certainly be different from every other, and that is why cognitive neuropsychology is the study of single cases, not data averaged across a group of patients. How then can generalization, a sine qua non of science, be achieved? It is achieved because all the patients are assumed to be performing with some damaged version of the same cognitive system. Thus, for example, the cognitive-neuropsychological evaluation of the model of reading in Figure 1 proceeds by investigating whether that model can account for all the reading symptoms seen in every patient with acquired dyslexia who comes along. If a patient reads in any way that could never be seen in the performance of any damaged version of the Figure a system, then that patient’s data is evidence against the model.

A brief history of cognitive neuropsychology

Cognitive neuropsychology first began to flourish in the second half of the Nineteenth Century, initially in relation to disorders in the comprehension and production of spoken language (aphasia). Continental neurologists such as Broca (1861), Lichtheim (1873) and Wernicke (1874) studied patients with aphasia and inferred information-processing models of the normal language-processing system from the patterns of preserved and impaired language abilities they saw in their patients. They even expressed these models as box-and-arrow flowcharts of information processing, which is the universal notation in modern cognitive neuropsychology (as in Figure 1). This cognitive-neuropsychological approach was also applied to the understanding of disorders of written language, both reading and spelling (Bastian, 1869; Dejerine, 1891), and soon spread to other cognitive domains such as object recognition (Lissauer, 1890), calculation (Lewandowsky & Stadelmann, 1908) and many others.

Cognitive neuropsychology was thus flourishing by the early Twentieth Century. But then it rapidly lost favour. This happened for two reasons, one to do with psychology and the other to do with neurology.

Re psychology: the whole idea that it is possible to study the structure and nature of mental information-processing systems - that is, the idea that it is possible to do cognitive psychology - was directly attacked by John B Watson in 1913 : "The time seems to have come", he wrote, " when psychology need no longer delude itself . . . into thinking that it is making mental states the object of observation. We have become so enmeshed in speculative questions concerning the elements of mind . . that I, as an experimental student, feel that something is wrong with our premises and the types of problems which develop from them." Watson argued that mental processes were not directly observable and therefore could not be studied scientifically. All that should be studied by psychologists is what could be objectively observed: stimuli and an organism's responses to them. This doctrine is known as behaviourism. It became very strong in the psychology of the first half of the twentieth century, and since it was completely incompatible with an interest in developing models of mental processing systems, it provided a hostile climate for cognitive psychology and hence for cognitive neuropsychology.

Re neurology: the nineteenth-century cognitive neuropsychologists were also neurologists. So they weren't satisfied just with developing modular models of cognitive processes. They also wanted to localize these modules in the brain. This was a hopelessly premature endeavour which was bound to fail, and when it failed this left them highly vulnerable to criticism. The endeavour was premature for two reasons. Firstly, the only way they could acquire information about the location in the brain of any patient's lesion was extremely crude - by autopsy after the patient's death. Secondly, even if the information about lesion location could have been obtained by less crude methods, the models themselves were not sufficiently detailed for questions to be sensibly asked about where the modules were located in the brain. That may even still be true even today; cognitive neuroscientists believe that it isn’t. Early in the twentieth century, a number of anti-modular and anti-localizationist neurologists attacked the work of Broca, Wernicke and others, and their attacks made highly effective use of the unconvincingness of the attempts by the nineteenth-century cognitive neuropsychologists to demonstrate relationships between particular lesion sites and particular cognitive impairments. Particularly effective were the attack on Broca by Pierre Marie in 1906 and, especially, the attack on the whole field of cognitive neuropsychology by Henry Head in 1926, which was expressed in the most brutal of terms: "Wernicke failed to recognize the wide-spread nature of the difficulty owing to the preconceptions with which it was approached: in the solemn discussion which follows that report we can only wonder at his clinical obtuseness and want of clinical insight . . We are astonished at the serene dogmatism with which the writers assume a knowledge of the working of the mind and its dependence on hypothetical groups of cells and fibres . . . Most of the observers mentioned in this chapter failed to contribute anything of permanent value to the solution of the problem."

The "Cognitive Revolution" - the abandonment of behaviourism and the acknowledgement that there are scientifically acceptable ways of investigating the structure and nature of mental information-processing systems even if these are no more directly observable than neutrons and electrons - occurred in Britain and North America in the mid-1950s. New and more detailed modular models of various forms of cognitive processing, initially language and also selective attention, were developed and applied to the explanation of data collected from experiments on normal subjects.

Then there developed certain research collaborations between cognitive psychologists who had been doing this kind of work and clinical neuropsychologists who saw in the clinic various kinds of breakdowns of cognition caused by brain damage. The clinicians were interested in understanding these breakdowns in more detail. The cognitive psychologists were interested in learning more about normal systems by studying how they could break down. The 1960s saw two such seminal collaborative papers, which marked the rebirth of cognitive neuropsychology: Marshall and Newcombe (1966) on reading and Warrington & Shallice (1969) on memory. A decade later, cognitive neuropsychology had been fully reestablished, according to Selnes (2001), who notes that in 1977 “a meeting to discuss deep dyslexia was convened in Oxford, and this is often considered by many to be a convenient marker for the early beginnings of cognitive neuropsychology (E. Saffran, personal communication, 2000). The book Deep Dyslexia (Coltheart, Patterson & Marshall, 1980) which resulted from the conference is considered by many to be the first major book that deals with the cognitive approach to neuropsychology. The journal Cognitive Neuropsychology was first published in 1984.” (Selnes, 2001, p. 38). Not long afterwards, in 1988, the field’s first textbook, Human Cognitive Neuropsychology, was published (Ellis & Young, 1988), and so was the first book critically reviewing the field (Shallice, 1988).

Applications

Cognitive neuropsychology has two major domains of application: assessment and rehabilitation.

Cognitive-neuropsychological assessment is assessment that is based on an explicit modular information-processing model of the relevant cognitive domain. The existence of the model permits the construction of tests specific to the individual modules of the model, so that a comprehensive analysis can be made of which of these cognitive modules is operating normally and which have been perturbed by brain damage (in the case of acquired disorders of cognition) or have not been acquired to age-appropriate levels (in the case of developmental disorders of cognition). The best-developed cognitive-neuropsychological assessment batteries are the PALPA battery for the assessment of disorders of spoken and written language (Kay, Lesser & Coltheart, 1992) and the BORB battery for the assessment of disorders of visual perception and visual object recognition (Riddoch and Humphreys, 1993).

Cognitive-neuropsychological rehabilitation (Coltheart, Brunsdon & Nickels, 2005) is similarly model-based: it is treatment that is specifically directed at improving the functioning of the particular cognitive modules or pathways that have been identified, via cognitive-neuropsychological assessment methods, as specifically impaired. Other approaches to neuropsychological rehabilitation differ from this in typically being rather generally aimed at the entire cognitive domain within which the patient shows some or other symptoms. Numerous examples of the cognitive-neuropsychological approach to rehabilitation can be found in Humphreys & Riddoch (1994) and Whitworth, Webster & Howard (2005).

Achievements

The volume by Coltheart and Caramazza (2006) is a recent review of the field which contains state-of-the-art accounts of contributions of cognitive neuropsychology to our understanding of a variety of domains of cognition, showcasing in particular what we have learned so far from cognitive neuropsychology about conceptual representation, speech production, sentence comprehension, reading and spelling, short-term memory, visual object recognition, spatial attention and skilled action.

References

Bastian, H. C. (1869). On the various forms of loss of speech in cerebral disease. British and Foreign Medical-Chirurgical Review, 43, 209-236, 470-492.

Rapp, B. (Ed.) (2001) Handbook of Cognitive Neuropsychology. New York: Psychology Press ISBN78-1-84169-044-5 (a set of chapters giving recent and authoritative overviews of most of the areas of cognitive neuropsychology).

Shallice, T. (1988). From Neuropsychology to Mental Structure. Cambridge: Cambridge University Press. ISBN0-521-31360-0. (contains important material on the history of the field and a critical analysis of the methods of cognitive neuropsychology)